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PubMedDate not supplied

[Clinical evaluation of the use of proglumide in the treatment of the peptic ulcer semebrome].

The authors have made a clinical evaluation of Proglumida in 27 patients suffering from Peptic ulcer. Proglumida was administered orraly, 2 tables of 200 mg 3 times a day, 1.200 mg in 24 hours, during a period varying from 21 to 28 days. The painful symptoms improved in 96% of the pain occurred in 59% during the first 7 days of treatment. The dispeptic symptoms improved in all cases, disappearing completely in 74%, but in a slower fashion than the pain, and in 68% of the cases only from the second week of treatment onward. The objectivation of the pain by palpation of the epigastrium improved in all cases and did so in a significant form in 59% of the cases during the first seven days of treatment. No undesireable side effects have been observed in any of the cases. We believe that Proglumida is a pharmacological drug of positive action in the treatment of the ulcer syndrome, because of its favorable action and the absence of secondary side effects.

Adolescent↗
PubMed1989

[Gastric acid secretion plays a role in food and water ingestion in mice].

The influence of blockade of the SAG on food and water intake was studied in the mouse. Proglumide (a gastrin receptor antagonist), the combination of proglumide plus cimetidine (inhibitor of the H2 histamine receptors), proglumide plus vagotomy and the simultaneous action of proglumide plus cimetidine plus vagotomy were used in order to get total inhibition of the gastric acid secretion. Statistical analysis shows that food intake experiences a significant increase by the action of proglumide, proglumide plus cimetidine, proglumide plus vagotomy and proglumide plus cimetidine plus vagotomy in comparison to the control group. However, water intake was significantly lower in proglumide plus cimetidine and proglumide plus vagotomy animals with respect to the other groups studied. In addition, proglumide plus cimetidine plus vagotomy increased significantly water intake in relation to the other groups studied. No changes were found in the body weight of the groups studied. We conclude that SAG plays a role in food and water intake in the mouse and both behaviors are interdependent processes.

Animals↗
PubMed2006

[Effects of gastrin receptor antagonist and cyclooxygenase-2 inhibitor on proliferation and apoptosis of gastric cancer cell].

OBJECTIVE: To investigate the regulative roles of the gastrin receptor antagonist proglumide and the specific cyclooxygenase (COX)-2 inhibitor NS-398 on the proliferation and apoptosis of gastric cancer cells. METHODS: Human gastric cancer cells of the line MKN-45 were routinely cultured in RPMI-1640 medium supplemented with 10% heat-inactivated fetal calf serum. Subconfluent cell cultures were treated with proglumide at a final concentration of 5 mmol/L, NS-398 at a final concentration of 10.0 micromol/L, or proglumide in combination with NS-398 for 48 h. The growth and proliferation of MKN-45 cells were analyzed with MTT assay. Flow cytometric analysis was used to detect the apoptosis of the gastric cancer cells. RT-PCR and Western blotting were used to detect the expression of apoptosis-inhibited gene bcl-2 mRNA and protein. RESULTS: The apoptosis rates of the cells treated by proglumide, NS-398, and combination of two agents were 24.7% +/- 3.2%, 26.7% +/- 3.4%, and 36.1% +/- 4.6% respectively, all significantly higher than that in the control group (1.6% +/- 0.6%, all P < 0.01). The apoptosis rates of the MKN-45 cells treated with proglumide combined with NS-398 was significantly greater than those of the cells treated by the two agents alone (both P < 0.05). Treatment with proglumide and NS-398 significantly reduced the bcl-2 mRNA and protein expression in the MKN-45 cells (P < 0.05). CONCLUSION: Both proglumide and NS-398 inhibit the proliferation and induce the apoptosis of human gastric cells. This apoptosis may be mediated by down-regulation of the expression of apoptosis-inhibited gene bcl-2. Co-treatment with proglumide and NS-398 have synergistic anticancer role.

Apoptosis↗
PubMed1985

Role of cholecystokinin in pancreatic exocrine response to intraluminal amino acids and fat.

Controversy continues over the relative contributions made by hormonal and neural mechanisms in the exocrine pancreatic response to ingested food. The recent description of the drug proglumide as a specific, competitive cholecystokinin (CCK)/gastrin receptor antagonist has permitted reevaluation of the role of CCK in this process. In chronic pancreatic fistula dogs, dose-response studies were performed to determine the effect of proglumide on the pancreatic responses to octapeptide of CCK (CCK-OP), intravenous bethanechol, intraduodenal amino acids, and intraduodenal fat. Pancreatic volume, protein, and bicarbonate outputs to all doses of CCK-OP were inhibited significantly (P less than 0.05) in a competitive manner, consistent with the proposed mode of action of proglumide. In contrast, proglumide caused only minor and insignificant inhibition of the output responses to intravenous bethanechol. Virtually complete inhibition to all doses of intraduodenal amino acids and fat was observed with proglumide administration. If indeed proglumide is a specific CCK receptor antagonist, these results support the hypothesis that CCK is the major mediator of the intestinal phase of exocrine pancreatic secretion.

Amino Acids↗
PubMed1989

[The effect of cholecystokinin antagonists on satiety induced by cholecystokinin octapeptide in dogs].

We administered two cholecystokinin antagonists to dogs intravenously (i.v.) and into the third cerebral ventricle (i.t.v.). Proglumide (3-300mg/kg/hr i.v. or 0.1-10mg/dog i.t.v.) reversed the satiety previously shown by mongrel dogs after i.t.v. CCK-8. A new glutaramic derivative, CR1409, blocked this satiety even more strongly when administered by either route. Proglumide increased proglumide levels in ventricular fluid, indicating its ability to cross the blood-brain barrier. However, i.t.v. proglumide did not appear in the blood during the observation period. These results suggest that systemic proglumide and CR1409 act as antagonists of the central CCK receptor concerning satiety in dogs; intravenously administered proglumide was found to cross the blood-brain barrier and partially but significantly reverse the satiety caused by CCK-8.

Animals↗
PubMed1980

The role of gastric mucosal hexosamine in aspirin-induced ulcers.

In order to elucidate the role of gastric tissue hexosamine, used as an index of mucopolysaccharide content, in the development and healing process of peptic ulcers, the distribution of hexosamine and the changes of gastric hexosamine content in the development and healing of aspirin-induced ulcers in rats were studied. In addition, the effects of proglumide and L-glutamine on gastric hexosamine were also studied. The hexosamine content was found to be the highest in the antrum, followed by the corpus and then the forestomach. The mucosa contained significantly higher hexosamine than the smooth muscle layer in both the antrum and the corpus. Prior treatment with proglumide significantly increased the mucosal hexosamine to the extent of 10.3--18.1% in the glandular stomach. Administration of aspirin decreased the gastric mucosal hexosamine and induced the onset of ulcer, while administration of proglumide suppressed the gastric lesions in proportion to dosage and correspondingly prevented a decrease of the hexosamine. In contrast, L-glutamine showed an anti-ulcerogenic effect without suppressing a decrease of the hexosamine. In the process of curing gastric lesions, proglumide accelerated the healing of the ulcers and simultaneously returned the total hexosamine content to its original level. These results suggest that the gastric mucosal hexosamine is closely related to the onset and healing of aspirin-induced ulcer in rats, and that proglumide contributes to both the prevention and healing of ulcers by increasing gastric mucosal hexosamine.

Animals↗
PubMed1988

The anti-CCK effect of glutaramic acid derivatives in anesthetized and conscious rats.

The effects of specific gastrin-cholecystokinin (CCK) receptor blockers (proglumide and a new, more potent product of Rotta Research Laboratorium, CR-1392) on pancreatic secretion were studied. Proglumide and CR-1392 caused a rightward and parallel shift, respectively, in the dose-response curve of CCK8 stimulated pancreatic protein secretion in anesthetized rats, demonstrating a competitive-like mechanism of inhibition. The mean PA2 values, demonstrating the 50% inhibitory dose of proglumide and CR-1392 were 3.7 and 5.7, respectively; i.e., CR-1392 proved to be about 100 times more potent than proglumide. In conscious rats, protein output and the volume of pancreatic juice were significantly decreased for about 2 h in response to 150 mg/kg of proglumide or 3 mg/kg of CR-1392 administered s.c. during diversion of pancreatic juice, demonstrating inhibition of endogenous CCK by glutaramic acid derivatives. Indeed, during reintroduction of precollected pancreatic juice into the duodenum, when the release of CCK is known to be almost totally eliminated, pancreatic secretion was not significantly modified by the same doses.

Anesthesia↗
PubMed1998

Cholecystokinin actions in the parabrachial nucleus: effects on thirst and salt appetite.

The present study investigated the effects of bilateral injections of the nonselective CCK receptor antagonist proglumide or CCK-8 into the lateral parabrachial nuclei (LPBN) on the ingestion of 0.3 M NaCl and water induced by intracerebroventricular injection of ANG II or by a combined treatment with subcutaneous furosemide (Furo) + captopril (Cap). Compared with the injection of saline (vehicle), bilateral LPBN injections of proglumide (50 micrograms . 200 nl-1 . site-1) increased the intake of 0.3 M NaCl induced by intracerebroventricular ANG II (50 ng/1 microliter). Bilateral injections of proglumide into the LPBN also increased ANG II-induced water intake when NaCl was simultaneously available, but not when only water was present. Similarly, the ingestion of 0.3 M NaCl and water induced by the treatment with Furo (10 mg/kg) + Cap (5 mg/kg) was increased by bilateral LPBN proglumide pretreatment. Bilateral CCK-8 (0.5 microgram . 200 nl-1 . site-1) injections into the LPBN did not change Furo + Cap-induced 0.3 M NaCl intake but reduced water consumption. When only water was available after intracerebroventricular ANG II, bilateral LPBN injections of proglumide or CCK-8 had no effect or significantly reduced water intake compared with LPBN vehicle-treated rats. Taken together, these results suggest that CCK actions in the LPBN play a modulatory role on the control of NaCl and water intake induced by experimental treatments that induce hypovolemia and/or hypotension or that mimic those states.

Animals↗